PerspectiveMolecular Biology

EZH2 Goes Solo

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Science  14 Dec 2012:
Vol. 338, Issue 6113, pp. 1430-1431
DOI: 10.1126/science.1232332

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Enhancer of zeste homolog 2 (EZH2), the catalytic subunit of Polycomb repressive complex 2 (PRC2), silences transcription through trimethylation of histone H3 lysine 27 (H3K27me3). EZH2 is frequently overexpressed in many cancer types, including breast, lung, and prostate cancer. EZH2 overexpression is also linked to poor survival, making it an important target in cancer therapy (1, 2). Prostate cancer can be treated by removal of testicular androgens, but androgen depletion is frequently associated with the recurrence of malignant neoplasms, defined as castration-resistant prostate cancer (CRPC), which has a poor prognosis. In prostate cancer, EZH2 represses the two tumor suppressor genes ADRB2 and DAB2IP (3, 4). However, on page 1465 of this issue, Xu et al. analyze the role of EZH2 in CRPC and report that the oncogenic function of EZH2 does not depend on gene silencing, but rather on transcriptional induction of a subset of its target genes (5).